Multifocal Ill-Defined Opacities

Bacterial Bronchopneumonia

Multiple areas of consolidation are the characteristic pattern of bacterial bronchopneumonia (see Fig 16.1 ; answer to question 1 is e ). Because this type of infection spreads via the tracheobronchial tree, large areas of air space consolidation are often preceded by lobular opacities ²³⁸ that tend to be ill defined because the fluid and inflammatory exudate that produce the opacities spread through the interstitial planes in addition to spilling into the alveolar spaces. ²³⁵ In some cases, the lobular pattern may have sharply defined borders where the exudate abuts an interlobular septum. The size of the radiologic opacities depends on the number of contiguous lobules involved. Intervening normal lobules lead to a very heterogeneous appearance. As the infection progresses, the consolidations will begin to coalesce and form a pattern of multilobar consolidation ( Fig 16.3 ) that may even become indistinguishable from the diffuse confluent pattern commonly associated with alveolar edema. This is a common pattern for hospital-acquired pneumonias.

The radiologic patterns of bronchopneumonia are determined by the virulence of the organism and the host’s defenses. The primary sites of injury are the terminal and respiratory bronchioles. The disease starts as an acute bronchitis and bronchiolitis. The large bronchi undergo epithelial destruction and infiltration of their walls by polymorphonuclear leukocytes. Epithelial destruction results in ulcerations that are covered with a fibrinopurulent membrane and that contain large quantities of multiplying organisms. As the inflammatory reaction spreads through the walls of the bronchioles to involve the alveolar walls, there is an exudation of fluid and inflammatory cells into the acinus, which results in the pattern of multifocal consolidations. As noted in Chapter 15 , patients with bronchopneumonia occasionally have only one lobe predominantly involved, but there are almost always other areas of involvement. An unusually virulent organism or failure of the patient’s immune response leads to rapid enlargement of the multifocal opacities and, finally, to diffuse air space consolidations. This has been observed in patients infected by common organisms and those infected with unusual organisms, including those with Legionnaires’ disease and those infected by Legionella micdadei (Pittsburgh pneumonia agent). 311, 436 With more aggressive organisms, such as Staphylococcus aureus and Pseudomonas , a necrotic bronchitis and bronchiolitis lead to thrombosis of lobular branches of the small pulmonary arteries, which accounts for the cavitation seen in necrotizing pneumonias such as methicillin-resistant Staphylococcus aureus (MRSA; see Chapter 24 ).

Septic Emboli

Septic emboli are another source of severe pulmonary infection that occurs when a bolus of infectious organisms are released into the blood and spread to the peripheral pulmonary vessels. The first radiologic signs of septic emboli are small, ill-defined peripheral opacities. As the infection spreads, the size of the opacities increases, leading to multifocal peripheral opacities. Septic embolization also has a high probability of cavitation, which makes it different from many of the other causes of this pattern. Clinical correlation is essential in the diagnosis of septic embolization. There should be a history of a significant febrile illness. Risk factors for septic embolism include sepsis, osteomyelitis, cellulitis, carbuncles, and right-sided endocarditis. Patients with right-sided endocarditis frequently have a history of intravenous drug abuse and are at increased risk for MRSA infection.

Viral Pneumonia

Viruses produce their effect in the epithelial cells of the respiratory tract, leading to tracheitis, bronchitis, and bronchiolitis. ²⁹⁵ The bronchial and bronchiolar walls become very edematous, congested, and infiltrated with lymphocytes. The bronchial infiltrate may extend into the surrounding peribronchial tissues, which become swollen. This infiltrate spreads into the septal tissues of the lung, leading to a diffuse, interstitial, mononuclear, cellular infiltrate. The changes in the airways may extend to the alveolar ducts, but most severe changes occur proximal to the terminal bronchioles. The adjacent alveolar cells, both type 1 and type 2, become swollen and detached. These surfaces then become covered with hyaline membranes. In fulminant cases, there are additional changes in the alveoli. The alveoli are filled with a mixture of blood, edema, fibrin, and macrophages. In the most severely affected areas, there is focal necrosis of the alveolar walls and thrombosis of the alveolar capillaries, leading to necrosis and hemorrhage.

The radiologic pattern of a viral pneumonia depends on both the virulence of the organism and host defenses. ⁵⁰ The mildest cases of viral infection are confined to the upper airways and manifest no radiologic abnormality. The earliest radiologic abnormalities are the signs of bronchitis and bronchiolitis, which may include peribronchial thickening and signs of air trapping. When the infection spreads into the septal tissues, a reticular pattern with interlobular septal lines may result, as described in Chapter 18 . The more serious cases lead to hemorrhagic edema and areas of air space consolidation. These opacities may be small and appear as a fine nodular pattern similar to that described in Chapter 17 , but the nodules tend to be less well defined than the classic miliary pattern. As the process spreads, lobular consolidations develop, as in bacterial bronchopneumonia. In the most severe cases, the lobular consolidations may coalesce into diffuse consolidation, resembling pulmonary edema or bacterial bronchopneumonia.

Influenza viral pneumonia should be suspected in patients with typical influenza symptoms of fever, dry cough, headache, myalgia, and prostration. As the infection spreads to the lower respiratory tract, the patient notices an increased production of sputum that may be associated with dyspnea, pleuritic chest pain, or both. Physical examination reveals rales that may be accompanied by diminished or harsh breath sounds. Because of the bronchial involvement, wheezes are occasionally noted. High-resolution computed tomography (HRCT) may reveal multifocal ground-glass opacities while the chest radiograph appears to be normal. The chest radiographic patterns evolve from a minimal reticular pattern to small, ill-defined nodules to lobular consolidations, and finally to diffuse confluent opacities. Influenza pneumonia may be complicated by adult respiratory distress syndrome or superimposed bacterial pneumonia. At this time, laboratory examination of the sputum and blood becomes paramount to rule out a superimposed bacterial bronchopneumonia. The organisms most likely to present a superimposed bacterial infection are pneumococci, staphylococci, streptococci, and H. influenzae. In this clinical setting, the development of a superimposed cavity virtually confirms a superimposed bacterial infection. Other causes of viral pneumonia are less commonly encountered in patients with normal immunity, but have been reported with hanta viruses, Epstein-Barr virus, adenoviruses, ²⁹⁵ and SARS. ⁴¹²

Fulminating cases of viral pneumonia are rarely encountered in patients with normal immunity but may occur in patients with suppressed immune systems including those receiving high-dose steroid therapy, patients receiving chemotherapy, patients with AIDS, organ transplant patients, pregnant women, and older adults. Herpes simplex, varicella, rubeola, cytomegaloviruses, and adenoviruses occur mainly in immunocompromised patients. ²⁹⁵

Varicella pneumonia characteristically occurs from 2 to 5 days after the onset of the typical rash. It is most commonly noted in infants, pregnant women, and adults with altered immunity. Approximately 10% of adult patients may have some degree of pulmonary involvement. In contrast to what is seen in bacterial pneumonias, sputum examination shows a predominance of mononuclear cells and giant cells. As in the consideration of other viral pneumonias, the possibility of superimposed bacterial infection is best excluded by laboratory examination of the sputum and blood. Because the viruses of herpes zoster and varicella are identical, patients with an atypical herpetic syndrome consisting of a rash with pain that follows the nerves of a single dermatome are also at increased risk for development of this type of pneumonia.

Rubeola (measles) pneumonia may be more difficult to diagnose by clinical criteria because the pneumonia occasionally precedes the development of the rash. As with other viral pneumonias, the clinical findings are nonspecific and consist of fever, cough, dyspnea, and minimal sputum production. Increasing sputum production requires exclusion of a superimposed bacterial pneumonia. Timing is important for evaluating a pneumonia associated with measles. The development of primary viral pneumonia in rubeola is synchronous with the first appearance of a rash, whereas secondary bacterial pneumonias are most likely to occur from 1 to 7 days after the onset of the rash. Bacterial infection is strongly suggested in the patient with a typical measles rash whose condition improves over a period of days before pneumonia develops. A third type of pneumonia associated with measles pneumonia is histologically referred to as giant cell pneumonia. This may follow overt measles in otherwise normal healthy children, but children with an altered immune system may develop subacute or chronic, but often fatal, pneumonias. Pathologically, giant cell pneumonia is characterized by an interstitial mononuclear infiltrate with giant cells.

Cytomegalic inclusion disease ² has few distinguishing clinical features, has a radiologic presentation suggestive of bronchopneumonia, and is frequently fatal in patients who are immunosuppressed. Histologically, the lung reveals a diffuse mononuclear interstitial pneumonia accompanied by considerable edema in the alveolar walls that may even spill into the alveolar spaces. In addition, the alveolar cells have characteristic intranuclear and intracytoplasmic occlusions. The radiologic opacities are the result of cellular infiltrates in the interstitium, as well as intra-alveolar hemorrhage and edema. Other viruses, including the coxsackie viruses, parainfluenza viruses, adenoviruses, and respiratory syncytial viruses, may result in disseminated multifocal opacities. When the course of the viral infection is mild, confirmation is rarely obtained during the acute phase of the disease, but may be made by viral culture or acute and convalescent serologic studies.